G
Gary S. Firestein
Researcher at University of California, San Diego
Publications - 372
Citations - 38435
Gary S. Firestein is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Arthritis & Synovial membrane. The author has an hindex of 92, co-authored 355 publications receiving 34907 citations. Previous affiliations of Gary S. Firestein include University of California, San Francisco & University of California, Berkeley.
Papers
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Journal ArticleDOI
NF-κB: a key role in inflammatory diseases
Paul P. Tak,Gary S. Firestein +1 more
TL;DR: The specificity of various NF-κB proteins, their role in inflammatory disease, the regulation of NF-β proteins and IκB activity by IκBs and IkkB kinase, and the development of therapeutic strategies aimed at inhibition are discussed.
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Evolving concepts of rheumatoid arthritis
TL;DR: Based on the pathogenic mechanisms, specific therapeutic interventions can be designed to suppress synovial inflammation and joint destruction in rheumatoid arthritis.
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HIF-1α Is Essential for Myeloid Cell-Mediated Inflammation
Thorsten Cramer,Yuji Yamanishi,Björn E. Clausen,Irmgard Förster,Rafal Pawlinski,Nigel Mackman,Volker H. Haase,Rudolf Jaenisch,Maripat Corr,Victor Nizet,Gary S. Firestein,Hans-Peter Gerber,Napoleone Ferrara,Randall S. Johnson +13 more
TL;DR: It is found that activation of HIF-1alpha is essential for myeloid cell infiltration and activation in vivo through a mechanism independent of VEGF, and its direct regulation of survival and function in the inflammatory microenvironment is demonstrated.
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Fibroblast-like synoviocytes: key effector cells in rheumatoid arthritis
Beatrix Bartok,Gary S. Firestein +1 more
TL;DR: Rheumatoid FLS develop a unique aggressive phenotype that increases invasiveness into the extracellular matrix and further exacerbates joint damage, and new agents that target FLS could potentially complement the current therapies without major deleterious effect on adaptive immune responses.
Journal ArticleDOI
c-Jun N-terminal kinase is required for metalloproteinase expression and joint destruction in inflammatory arthritis
Zuoning Han,David L. Boyle,Lufen Chang,Brydon L. Bennett,Michael Karin,Li Yang,Anthony M. Manning,Gary S. Firestein +7 more
TL;DR: The novel JNK inhibitor SP600125 completely blocked IL-1--induced accumulation of phospho-Jun and induction of c-Jun transcription in synoviocytes and in joint arthritis, indicating that JNK is an important therapeutic target for RA.